A 70-year-old female with a history of hypertension and dyslipidemia was admitted with non-ST elevation acute coronary syndrome (NSTE-ACS) to the provincial hospital. Her blood pressure was 135/85 mmHg, her heart rate was 70 beats per minute, her respiration rate was 22 breaths per minute, and her temperature was 36.5 ^oC. The angiography at the provincial hospital showed TVD with LM. The patient was advised to undergo CABG, but she strongly refused. She was referred for PCI at our institution.

The initial electrocardiogram showed a sinus rhythm rate of 70 bpm with symmetrical T wave inversion in V1 to V3, suggestive of NSTE-ACS. The transthoracic echocardiography revealed a left ventricular ejection fraction (LVEF) of 45% with anterior and anteroseptal wall hypokinesia from mid to apex and no significant valvular abnormalities. The high-sensitivity troponin T at the emergency department was elevated at 1,750 ng/mL (normal range:<13.9 ng/mL). Other laboratory results were normal.

Urgent coronary angiography at the provincial hospital revealed critical stenosis of the distal LM, which is suspicious of a calcified nodule, significant stenosis at the proximal to midLAD, 50% stenosis at the mid LCx, and borderline stenosis at the proximal to mid RCA. Multiple angiogram views were injected to determine the severity of stenosis at the ostial LCx. However, the severity of stenosis at the ostial LCx could not be determined by the multiple angiogram views.

 Due to the indefinite diagnosis of the lesion at LM and the unclarified degree of stenosis of ostial LCx, IVUS was performed in LM, LAD, and LCx. We engaged LM with a 7Fr EBU via RFA.IVUS from LM to LAD showed eruptive calcified nodules at LM with MLA 2.1 mm2 and fibrocalcific plaque with MLA 2.6 mm2 at proximal to mid LAD. IVUS from LM to LCx showed critical stenosis at ostial LCx with eruptive calcified nodules with MLA 2.1 mm2. We planned to perform PCI at LM bifurcation (Medina 1-1-1) with the double-kissing Culotte technique and prepare the lesion with the cutting balloon due to the IVUS calcium score being 1. LM, proximal LAD, and proximal LCx lesions were dilated with a semi-compliant 2.5/15 mm balloon at 18 atm and a cutting balloon 3.5/10 mm at 14 atm. IVUS after pre-dilatation showed a shift of eruptive calcified nodules to the vessel wall and increased diameter of the LM, proximal LAD, and LCx. A 3.0/36 mm stent was deployed from LM to LAD. The proximal optimization technique (POT) was performed with a non-compliant 4.5/8 mm balloon at 20 atm. The kissing balloon was performed with non-compliant 3.5/15 mm balloons at 8 atm. A 3.0/19 mm stent was deployed from LM to LCx. POT was performed with a non-compliant 4.5/8 mm balloon at 20 atm. The kissing balloon was performed with non-compliant 3.5/15 mm balloons at 8 atm. Final POT with a non-compliant 4.5/8 mm balloon at 24 atm. IVUS post-PCI showed MSA 15.6 mm2 of LM, MSA 9.3 mm2 of LAD, and MSA 8.1 mm2 of LCx.

This is a case of ACS caused by the eruptive calcified nodules at LM. CABG is the treatment of choice for revascularization in this patient; however, she denied CABG. The DK culotte technique with IVUS guidance for LM bifurcation PCI was successfully performed.In high-risk complex cases, IVUS is useful in the definitive diagnosis of ambiguous lesions, determining the most suitable technique for plaque modification prior to stenting, and determining the optimal strategy for LM bifurcation angioplasty. Some of the eruptive calcified nodules can be deformed by a balloon-based strategy. However, the incidence rate of target lesion failure is higher than that of non-eruptive calcified nodules.